Oncotarget · 2026
Case Report WIN-MTB-2024001 - WIN International Molecular Tumor Board: A 55-year-old male with glioblastoma exhibiting amplifications in MDM2 and EGFR.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
El-Deiry Wafik S, Ikeda Sadakatsu, Magidi Shai, Bresson Catherine, Abdel-Razeq Hikmat, Joshua Anthony, Hernando-Calvo Alberto, Oberoi Arjun, Hu Zhihuang, Meissner Tobias, Elsey Rachel, Al-Omari Amal, Wunder Fanny, Kurzrock Razelle
Аннотация
Copyright: © 2026 El-Deiry et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The WIN Consortium International Molecular Tumor Board brings together precision oncology experts from 18 organizations in 13 countries across four continents and provides discussion for patients with cancer across the world. This case report details the medical journey of a 55-year-old man diagnosed with high-grade glioblastoma (GBM), characterized by amplifications of MDM2 and EGFR, alongside other critical genomic alterations, including a CDKN2A frameshift mutation. Despite the aggressive nature of GBM, the patient was in remission following a combination of radiotherapy and chemotherapy, surgery and participation in a phase II clinical trial (PI3K/mTOR inhibitor) combined with ketogenic diet and metformin. However, the patient was also considering personalized neoantigen vaccine therapy targeting tumor-specific mutated peptides as part of his treatment strategy. This case underscores the immense complexity of treating GBM. Next generation sequencing showed MDM2 amplification, which hinders the tumor-suppressive functions of p53, and EGFR amplification, which promotes oncogenic signaling. The experts highlighted various therapeutic options discussed in the event of relapse: EGFR inhibitors, various MDM2 inhibitors, and personalized combination therapies targeting both EGFR and CDK4/6. Additionally, the Molecular Tumor Board discussed the reported risk of resistance or hyper-progression with immune checkpoint blockade in the presence of EGFR and MDM2 alterations. Innovative approaches such as combining MDM2 and EGFR inhibitors with immunotherapy, as well as the use of teserpaturev, a genetically engineered herpes simplex virus were addressed. This case emphasizes the importance of personalized treatment strategies for GBM and the need for ongoing clinical research to explore novel therapeutic options.